Drugs that are used to treat RHEUMATOID ARTHRITIS.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907)
A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970)
An oral chrysotherapeutic agent for the treatment of rheumatoid arthritis. Its exact mechanism of action is unknown, but it is believed to act via immunological mechanisms and alteration of lysosomal enzyme activity. Its efficacy is slightly less than that of injected gold salts, but it is better tolerated, and side effects which occur are potentially less serious.
Organic compounds that contain GOLD as an integral part of the molecule. Some are used as ANTIRHEUMATIC AGENTS. The term chrysotherapy derives from an ancient Greek term for gold.
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.
A variable mixture of the mono- and disodium salts of gold thiomalic acid used mainly for its anti-inflammatory action in the treatment of rheumatoid arthritis. It is most effective in active progressive rheumatoid arthritis and of little or no value in the presence of extensive deformities or in the treatment of other forms of arthritis.
Therapy with two or more separate preparations given for a combined effect.
A subspecialty of internal medicine concerned with the study of inflammatory or degenerative processes and metabolic derangement of connective tissue structures which pertain to a variety of musculoskeletal disorders, such as arthritis.
3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
Roentgenography of a joint, usually after injection of either positive or negative contrast medium.
Also known as articulations, these are points of connection between the ends of certain separate bones, or where the borders of other bones are juxtaposed.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
A type of inflammatory arthritis associated with PSORIASIS, often involving the axial joints and the peripheral terminal interphalangeal joints. It is characterized by the presence of HLA-B27-associated SPONDYLARTHROPATHY, and the absence of rheumatoid factor.
The articulations extending from the ANKLE distally to the TOES. These include the ANKLE JOINT; TARSAL JOINTS; METATARSOPHALANGEAL JOINT; and TOE JOINT.
Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The articulations extending from the WRIST distally to the FINGERS. These include the WRIST JOINT; CARPAL JOINTS; METACARPOPHALANGEAL JOINT; and FINGER JOINT.
Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.
A plant genus of the family CELASTRACEAE that is a source of triterpenoids and diterpene epoxides such as triptolide.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Inflammation of a synovial membrane. It is usually painful, particularly on motion, and is characterized by a fluctuating swelling due to effusion within a synovial sac. (Dorland, 27th ed)
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
An agency of the PUBLIC HEALTH SERVICE established in 1990 to "provide indexing, abstracting, translating, publishing, and other services leading to a more effective and timely dissemination of information on research, demonstration projects, and evaluations with respect to health care to public and private entities and individuals engaged in the improvement of health care delivery..." It supersedes the National Center for Health Services Research. The United States Agency for Health Care Policy and Research was renamed Agency for Healthcare Research and Quality (AHRQ) under the Healthcare Research and Quality Act of 1999.
A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.
Antibodies produced by a single clone of cells.
The inner membrane of a joint capsule surrounding a freely movable joint. It is loosely attached to the external fibrous capsule and secretes SYNOVIAL FLUID.
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
Measurement of rate of settling of erythrocytes in anticoagulated blood.
Substances that reduce or suppress INFLAMMATION.
A chronic inflammatory condition affecting the axial joints, such as the SACROILIAC JOINT and other intervertebral or costovertebral joints. It occurs predominantly in young males and is characterized by pain and stiffness of joints (ANKYLOSIS) with inflammation at tendon insertions.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Complex pharmaceutical substances, preparations, or matter derived from organisms usually obtained by biological methods or assay.
Arthritis of children, with onset before 16 years of age. The terms juvenile rheumatoid arthritis (JRA) and juvenile idiopathic arthritis (JIA) refer to classification systems for chronic arthritis in children. Only one subtype of juvenile arthritis (polyarticular-onset, rheumatoid factor-positive) clinically resembles adult rheumatoid arthritis and is considered its childhood equivalent.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Surveillance of drugs, devices, appliances, etc., for efficacy or adverse effects, after they have been released for general sale.
An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression.
Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
The joint that is formed by the distal end of the RADIUS, the articular disc of the distal radioulnar joint, and the proximal row of CARPAL BONES; (SCAPHOID BONE; LUNATE BONE; triquetral bone).
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
A measure of the quality of health care by assessment of unsuccessful results of management and procedures used in combating disease, in individual cases or series.
The articulation between the head of one phalanx and the base of the one distal to it, in each finger.
Therapeutic act or process that initiates a response to a complete or partial remission level.
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
Methods to determine in patients the nature of a disease or disorder at its early stage of progression. Generally, early diagnosis improves PROGNOSIS and TREATMENT OUTCOME.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Forceful administration under the skin of liquid medication, nutrient, or other fluid through a hollow needle piercing the skin.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Combinations of diagnostic or therapeutic substances linked with specific immune substances such as IMMUNOGLOBULINS; MONOCLONAL ANTIBODIES; or ANTIGENS. Often the diagnostic or therapeutic substance is a radionuclide. These conjugates are useful tools for specific targeting of DRUGS and RADIOISOTOPES in the CHEMOTHERAPY and RADIOIMMUNOTHERAPY of certain cancers.
Elements of limited time intervals, contributing to particular results or situations.
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
A yellow metallic element with the atomic symbol Au, atomic number 79, and atomic weight 197. It is used in jewelry, goldplating of other metals, as currency, and in dental restoration. Many of its clinical applications, such as ANTIRHEUMATIC AGENTS, are in the form of its salts.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures.
Determination of the degree of a physical, mental, or emotional handicap. The diagnosis is applied to legal qualification for benefits and income under disability insurance and to eligibility for Social Security and workmen's compensation benefits.
Research techniques that focus on study designs and data gathering methods in human and animal populations.
A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.
A plasma protein that circulates in increased amounts during inflammation and after tissue damage.
A class of statistical methods applicable to a large set of probability distributions used to test for correlation, location, independence, etc. In most nonparametric statistical tests, the original scores or observations are replaced by another variable containing less information. An important class of nonparametric tests employs the ordinal properties of the data. Another class of tests uses information about whether an observation is above or below some fixed value such as the median, and a third class is based on the frequency of the occurrence of runs in the data. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1284; Corsini, Concise Encyclopedia of Psychology, 1987, p764-5)
Any dummy medication or treatment. Although placebos originally were medicinal preparations having no specific pharmacological activity against a targeted condition, the concept has been extended to include treatments or procedures, especially those administered to control groups in clinical trials in order to provide baseline measurements for the experimental protocol.
A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.
Patterns of practice related to diagnosis and treatment as especially influenced by cost of the service requested and provided.

Dose-loading with hydroxychloroquine improves the rate of response in early, active rheumatoid arthritis: a randomized, double-blind six-week trial with eighteen-week extension. (1/3077)

OBJECTIVE: To investigate the usefulness of hydroxychloroquine (HCQ) dose-loading to increase the percentage of responders or rate of response in treating rheumatoid arthritis (RA). METHODS: Two hundred twelve patients with early RA (mean duration 1.5 years) were enrolled in a 24-week trial. Patients were stabilized with 1,000 mg naproxen/day and then began a 6-week, double-blind trial comparing treatment with HCQ at 400 mg/day (n = 71), 800 mg/day (n = 71), and 1,200 mg/day (n = 66), followed by 18 weeks of open-label HCQ treatment at 400 mg/day. RESULTS: All patients had mild, active disease at the time of initiation of HCQ treatment (31-43% rheumatoid factor positive; no previous disease-modifying antirheumatic drugs; mean swollen joint count 8.6-10.4). Based on the Paulus criteria, response during the 6-week double-blind portion of the study was 47.97%, 57.7%, and 63.6% in the 400 mg/day, 800 mg/day, and 1,200 mg/day groups, respectively (P = 0.052). Discontinuations for adverse events were dose related (3 in the 400 mg/day group, 5 in the 800 mg/day group, 6 in the 1,200 mg/day group). Most involved the gastrointestinal (GI) system, with the background naproxen treatment possibly contributing. Ocular abnormalities occurred in 17 of 212 patients (8%) but were not dose related. CONCLUSION: Dose-loading with HCQ increased the degree of response at 6 weeks in this group of patients with early, predominantly seronegative RA. Adverse GI events were dose related, while adverse ocular events were not.  (+info)

Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose. (2/3077)

Gold compounds have long been used in the treatment of rheumatoid arthritis (RA). However, their actions in RA have not been clarified. In this study, we examined the effect of one of the monovalent gold compounds, aurothioglucose (AuTG), on the IL-1-induced production of IL-6, IL-8 and granulocyte macrophage colony stimulating factor (GM-CSF) from rheumatoid synovial fibroblasts (RSF) isolated from three RA patients. IL-6 and IL-8 induction but not GM-CSF induction was inhibited in most of the RSF after pretreatment with AuTG. Since gene expression of these cytokines is known to be under the control of a common transcription factor, NF-kappaB, the effect of AuTG on the cellular localization of NF-kappaB (p65 subunit) and on NF-kappaB-DNA binding was examined. Although AuTG treatment did not prevent NF-kappaB nuclear translocation, AuTG blocked the DNA-binding activity of NF-kappaB when examined in vitro. Morphologically, both metal-specific cell staining using p-dimethylaminobenzylidene rhodamine and transmission electron microscopic examinations demonstrated the accumulation of metal gold in the cytoplama and some organella (mitochondria and lysosomes) of the AuTG-treated RSF. These results indicate that one of the anti-rheumatic actions of AuTG might be through its inhibitory action on NF-kappaB.  (+info)

Efficacy of sustained blood levels of interleukin-1 receptor antagonist in animal models of arthritis: comparison of efficacy in animal models with human clinical data. (3/3077)

OBJECTIVE: To determine the role of interleukin-1 receptor antagonist (IL-1Ra) in rat adjuvant arthritis and rat type II collagen-induced arthritis, and to compare the efficacy in rat models with that seen in human clinical trials of IL-1Ra. METHODS: Rats with developing adjuvant arthritis or established collagen-induced arthritis were treated with IL-1Ra by continuous infusion in order to determine and maintain efficacious blood levels of this IL-1 inhibitory protein in the rats for comparison with human clinical data. The effects of treatment in the rats were monitored by sequential caliper measurement of the ankle joints, determination of final paw weights, and histologic evaluation with particular emphasis on bone and cartilage lesions. The effects of IL-1Ra on joint swelling and radiographic bone damage in patients with rheumatoid arthritis (RA) in a 6-month trial were compared with the findings in rats. RESULTS: Dramatic differences in the profile of IL-1Ra activity were seen between the 2 groups of rats. Modest antiinflammatory effects were observed in the adjuvant arthritis rats treated with IL-1Ra. However, marked inhibition of bone resorption occurred, even at doses with which antiinflammatory activity was not seen. In contrast, IL-1Ra treatment of rats with established collagen-induced arthritis resulted in nearly complete suppression of all aspects of the disease when adequate blood levels of IL-1Ra were maintained. Treatment of RA patients with IL-1Ra (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. CONCLUSION: IL-1 appears to be of major importance in mediating the bone resorption that occurs in rat adjuvant arthritis, but is less important in the pathogenesis of periarticular inflammation in this disease. In contrast, IL-1 is of major importance in mediating all aspects of disease progression in rat collagen-induced arthritis. Similar to the response in adjuvant arthritic rats, RA patients treated with IL-1Ra showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. However, a comparison of the plasma levels of IL-1Ra in humans and rats suggests that the optimal level of dosing for continuous saturation of IL-1 receptors may not have been achieved in humans, although this was achieved in the rat studies.  (+info)

Effect of its demethylated metabolite on the pharmacokinetics of unchanged TAK-603, a new antirheumatic agent, in rats. (4/3077)

A factor in the dose-dependent pharmacokinetics of ethyl 4-(3, 4-dimethoxyphenyl)-6,7-dimethoxy-2-(1,2, 4-triazol-1-yl-methyl)quinoline-3-carboxylate (TAK-603) in rats was shown to be due to the inhibition of metabolic clearance of unchanged TAK-603 by its major metabolite, M-I, in other words, product inhibition. The effect of M-I on the metabolic clearance of TAK-603 was studied using rats continuously infused i.v. with this metabolite at rates of 5.3 and 16.0 mg/h/kg. The total body clearance of TAK-603 was decreased remarkably in M-I-infused rats, and the decline of total body clearance depended on the steady-state plasma concentrations of M-I. The effect of M-I generated from the dosed parent drug on the plasma concentration-time profile of TAK-603 was investigated using bile-cannulated rats after i.v. injection of 14C-labeled TAK-603 at doses of 1 and 15 mg/kg. Elimination rates of TAK-603 from rat plasma increased in the bile-cannulated rats in which systemic M-I levels were reduced by interrupting its enterohepatic circulation. To express, simultaneously, the relationships between TAK-603 and M-I in plasma concentration-time profiles, a kinetic model based on the product inhibition was developed for the bile-cannulated rats. A good agreement between calculated curves and the observed concentrations of both TAK-603 and M-I was found at 1 and 15 mg/kg, and the calculated curves were drawn using constant parameters for the two dosages. These results show that the product inhibition by M-I is one factor responsible for the dose-dependent pharmacokinetics of TAK-603 in rats.  (+info)

High and low molecular weight DNA cleavage in ovarian granulosa cells: characterization and protease modulation in intact cells and in cell-free nuclear autodigestion assays. (5/3077)

To continue elucidation of the biochemical and molecular pathways involved in the induction of apoptosis in granulosa cells (GC) of ovarian follicles destined for atresia, we characterized the occurrence and protease modulation of high and low molecular weight (MW) DNA fragmentation during rat GC death. Atresia of ovarian follicles, occurring either spontaneously in vivo or induced in vitro, was associated with both high MW and internucleosomal (low MW) DNA cleavage. Incubation of follicles in the presence of a putative irreversible and non-competitive inhibitor of caspase-1 (interleukin-1beta-converting enzyme or ICE), sodium aurothiomalate (SAM), completely prevented internucleosomal, but not high MW, DNA cleavage. As reported previously, morphological features of apoptosis (pyknosis, cellular condensation) and atresia (granulosa cell disorganization, oocyte pseudomaturation) remained detectable in SAM-treated follicles. The potential involvement of proteases in endonuclease activation was further analyzed in cell-free assays using nuclei from both GC (which autodigest their DNA) and HeLa cells (HC, which do not autodigest their DNA unless incubated with extracts prepared from other cell types). Crude cytoplasmic extracts prepared from GC induced both high MW and internucleosomal DNA cleavage in HC nuclei. The induction of low, but not high, MW DNA cleavage in HC nuclei by GC extracts was suppressed by pretreatment of the extracts with SAM or with any one of the serine protease inhibitors, dichloroisocoumarin (DCI), N-tosyl-L-leucylchloromethylketone (TLCK) or N-tosyl-L-phenylchloromethylketone (TPCK). Interestingly, SAM and DCI also prevented cation-induced low MW DNA fragmentation in GC nuclei; however, TLCK and TPCK were without effect. Our results support a role for cytoplasmic and nuclear serine proteases in the activation of the endonuclease(s) responsible for internucleosomal DNA cleavage during apoptosis.  (+info)

Prospective six year follow up of patients withdrawn from a randomised study comparing parenteral gold salt and methotrexate. (6/3077)

OBJECTIVE: To confirm the impression of a better outcome of patients withdrawn from parenteral gold salt therapy compared with those withdrawn from methotrexate. METHODS: Patients with early, active, and erosive RA were randomised for a double blind trial to receive either weekly 15 mg intramuscular methotrexate or 50 mg goldsodiumthiomalate. If the drug had to be withdrawn because of side effects treatment was continued with the other drug in still active disease. Patients with insufficient response were treated with a combination of both drugs. All patients were followed up by an extended clinical and radiographic evaluation. RESULTS: 64 patients each were allocated to methotrexate and gold treatment. After 72 months a complete record was available for 88% of patients. Within the first 36 months 38 patients withdrew from gold treatment (95% because of side effects) and 23 patients withdrew from methotrexate (57% because of side effects). A significant 40% to 70% improvement of all parameters (erythrocyte sedimentation rate, C reactive protein, swollen and tender joints, radiological progression) compared with baseline was observed in patients completing their randomised treatment with gold or methotrexate. The same improvement over three years was seen in patients who withdrew from gold treatment, while patients withdrawing from methotrexate experienced a deterioration of their disease. CONCLUSION: Withdrawals represent the majority of patients in long term drug trials. Patients with early RA stopping gold because of side effects show almost the same sustained improvement as patients continuing gold or methotrexate. Patients withdrawn from methotrexate experience a reactivation of their disease.  (+info)

Does sulphasalazine cause drug induced systemic lupus erythematosus? No effect evident in a prospective randomised trial of 200 rheumatoid patients treated with sulphasalazine or auranofin over five years. (7/3077)

BACKGROUND: Sulphasalazine (SSZ) has been reported to cause drug induced systemic lupus erythematosus (SLE), but diagnosis of this complication in the context of rheumatoid arthritis (RA) is difficult. OBJECTIVE: To determine prospectively: (1) if patients become seropositive for antinuclear antibodies (ANA) during prolonged treatment with SSZ without clinical evidence of SLE; (2) if ANA positive patients develop more adverse reactions than ANA negative patients; (3) if drug induced SLE was identified in this cohort. METHODS: 200 patients enrolled in a randomised prospective trial of SSZ and auranofin (AUR) were followed up for five years. Baseline and annual ANA results were collected along with information on drug toxicity and reasons for discontinuation of treatment. RESULTS: Over five years 24 patients stopped taking SSZ and 49 AUR because of side effects. Of the features common to SLE, rash developed in nine SSZ patients and 11 AUR treated patients and mouth ulcers in three and four patients respectively. Six SSZ treated patients and three treated with AUR developed leucopenia, which promptly resolved with drug withdrawal. No adverse event was ascribed to drug induced SLE. Of the 72 SSZ treated patients who were ANA negative or weakly positive at outset, 14 (19%) became strongly ANA positive compared with 11 (14%) of 80 AUR patients. Patients ANA positive at baseline or who became ANA positive were not more likely to develop drug toxicity or to withdraw from treatment than those ANA negative throughout. CONCLUSION: ANA positivity is common in patients with RA, but the presence or development of ANA did not increase the likelihood of withdrawing from treatment. No case of drug induced SLE was seen over five years in this study.  (+info)

In vivo transfer of interleukin-1 receptor antagonist gene in osteoarthritic rabbit knee joints: prevention of osteoarthritis progression. (8/3077)

The goal of this study was to determine the efficacy of local IL-1Ra gene therapy by intra-articular plasmid injections on structural changes in the meniscectomy rabbit model of osteoarthritis. A partial meniscectomy of the right knee was performed on the rabbits through a medial parapatellar incision. The rabbits were then divided into four experimental groups. Group 1 received no treatment. Group 2 received three consecutive intra-articular injections at 24-hour intervals of 0.9% saline containing a lipid, gammaAP-DLRIE/DOPE, and a DNA plasmid, VR1012. Group 3 received three consecutive injections of saline containing 1000 microg of canine IL-1Ra plasmid and lipid. The injections were given starting 4 weeks post-surgery. Rabbits from Group 1 were killed 4 weeks post-surgery, and all other rabbits 8 weeks post-surgery. The severity of macroscopic and microscopic changes on cartilage on the medial and femoral condyles and tibial plateaus and synovium were graded separately. Specimens were also processed for immunohistochemical staining using a rabbit polyclonal antibody against canine IL-1Ra. The level of canine IL-1Ra in synovial fluid was determined using enzyme-linked immunosorbent assay. The presence of the DNA plasmid in the synovium was tested by polymerase chain reaction. A significant reduction in the width of osteophytes and size of macroscopic lesions (P < 0.04) was observed, and was dependent on the amount of IL-1Ra plasmid injected. A significant reduction was also noted in the severity of histologic cartilage lesions (P < 0.01) in the group that received the highest dosage (1000 microg) of IL-1Ra plasmid. IL-1Ra was detected in synovial fluid by enzyme-linked immunosorbent assay and by immunohistochemical staining in the synovium and cartilage of rabbits that received injections containing the IL-1Ra plasmid. Polymerase chain reaction analysis of synovial DNA revealed the presence of the cloned cDNA dog IL-1Ra up to 4 weeks after the first intra-articular injection. This study demonstrates that direct in vivo transfer of the IL-1Ra gene into osteoarthritis knee cells using intra-articular injections of a plasmid vector and lipids can significantly reduce the progression of experimental osteoarthritis. This avenue may therefore represent a promising future treatment for osteoarthritis.  (+info)

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

There are five types of PsA:

1. Asymptomatic psoriatic arthritis - This type of psoriatic arthritis does not cause any symptoms and is typically diagnosed during routine blood tests or imaging studies.

2. Symptomatic psoriatic arthritis - This type of psoriatic arthritis causes painful joints, stiffness, and swelling in the hands and feet.

3. Distal interphalangeal predominant psoriatic arthritis - This type of psoriatic arthritis affects the joints at the tips of the fingers and toes.

4. Polyarticular psoriatic arthritis - This type of psoriatic arthritis causes inflammation in multiple joints throughout the body, including the hands, feet, knees, elbows, and spine.

5. Sulfur-shoulder psoriatic arthritis - This type of psoriatic arthritis primarily affects the shoulders and upper back.

Symptoms of PsA may include:

1. Joint pain and stiffness

2. Swollen and warm joints

3. Redness and warmth in the affected area

4. Fatigue

5. Low-grade fever

6. Loss of range of motion

7. Skin rashes or lesions

PsA is diagnosed based on a combination of physical examination, medical history, and laboratory tests such as blood tests to check for inflammatory markers (e.g., ESR and CRP) and X-rays or imaging studies to assess joint damage. There is no cure for PsA, but various treatments can help manage symptoms, slow the progression of the disease, and improve quality of life. These may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs) or biologic agents that target specific proteins involved in inflammation. In severe cases, surgery may be necessary to repair damaged joints or correct deformities.

It's important for people with PsA to work closely with their healthcare provider to develop a personalized treatment plan that addresses their individual needs and monitors their disease activity over time. With appropriate treatment and self-care, many people with PsA are able to manage their symptoms, maintain joint function, and lead active and fulfilling lives.

In conclusion, psoriatic arthritis (PsA) is a chronic inflammatory disease that affects both the skin and joints, causing pain, stiffness, and swelling in various parts of the body. Early diagnosis and appropriate treatment can help manage symptoms, slow the progression of the disease, and improve quality of life.

1. Rheumatoid arthritis (RA): An autoimmune disease that causes inflammation in the joints, leading to pain, stiffness, and swelling.
2. Osteoarthritis (OA): A degenerative condition that occurs when the cartilage in the joints wears down over time, causing pain and stiffness.
3. Psoriatic arthritis (PsA): An inflammatory disease that affects both the skin and joints, often occurring in people with psoriasis.
4. Ankylosing spondylitis (AS): A condition that causes inflammation in the spine and peripheral joints, leading to stiffness and pain.
5. Lupus: An autoimmune disease that can affect multiple systems in the body, including the joints, skin, and kidneys.
6. Juvenile idiopathic arthritis (JIA): A condition that affects children under the age of 16, causing inflammation in the joints and potentially leading to long-term complications.
7. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dryness in the eyes and mouth.
8. Fibromyalgia: A condition characterized by widespread pain, fatigue, and sleep disturbances.
9. Gout: A type of inflammatory arthritis caused by excessive levels of uric acid in the blood, leading to sudden and severe attacks of joint pain.
10. Osteoporosis: A condition characterized by brittle bones and an increased risk of fractures, often occurring in older adults.

Rheumatic diseases can be challenging to diagnose and treat, as they often involve complex symptoms and a range of possible causes. However, with the help of rheumatology specialists and advanced diagnostic tools, it is possible to manage these conditions effectively and improve quality of life for patients.

Osteoarthritis (OA) is a degenerative condition that occurs when the cartilage that cushions the joints breaks down over time, causing the bones to rub together. It is the most common form of arthritis and typically affects older adults.

Rheumatoid arthritis (RA) is an autoimmune condition that occurs when the body's immune system attacks the lining of the joints, leading to inflammation and pain. It can affect anyone, regardless of age, and is typically seen in women.

Other types of arthritis include psoriatic arthritis, gouty arthritis, and lupus-related arthritis. Treatment for arthritis depends on the type and severity of the condition, but can include medications such as pain relievers, anti-inflammatory drugs, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy and lifestyle changes, such as exercise and weight loss, can also be helpful. In severe cases, surgery may be necessary to repair or replace damaged joints.

Arthritis is a leading cause of disability worldwide, affecting over 50 million adults in the United States alone. It can have a significant impact on a person's quality of life, making everyday activities such as walking, dressing, and grooming difficult and painful. Early diagnosis and treatment are important to help manage symptoms and slow the progression of the disease.

There are several possible causes of synovitis, including:

1. Infection: Bacterial, viral, or fungal infections can cause synovitis.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis, psoriatic arthritis, and gout can cause chronic synovitis.
3. Overuse injuries: Repetitive strain injuries, such as those caused by repetitive jumping or throwing, can lead to synovitis in the affected joint.
4. Trauma: A sudden injury, such as a fall or a blow to the joint, can cause acute synovitis.

Symptoms of synovitis may include:

1. Pain: Pain is the most common symptom of synovitis, and it can range from mild to severe.
2. Swelling: The affected joint or limb may become swollen and warm to the touch.
3. Limited range of motion: Synovitis can cause stiffness and limited mobility in the affected joint.
4. Redness: The affected area may become red and inflamed.
5. Fever: In some cases, synovitis may be accompanied by a fever.

Treatment for synovitis depends on the underlying cause and the severity of the condition. Conservative treatments such as rest, physical therapy, and anti-inflammatory medications are often effective in managing mild to moderate cases of synovitis. In more severe cases, surgical intervention may be necessary.

In conclusion, synovitis is a common condition that can cause pain and limited mobility in the affected joint or limb. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help to prevent long-term damage and improve outcomes.

Spondylitis, ankylosing can affect any part of the spine, but it most commonly affects the lower back (lumbar spine) and the neck (cervical spine). The condition can also affect other joints, such as the hips, shoulders, and feet.

The exact cause of spondylitis, ankylosing is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissue in the joints. Genetics may also play a role in the development of the condition.

Symptoms of spondylitis, ankylosing can include:

* Back pain and stiffness
* Pain and swelling in the joints
* Limited mobility and flexibility
* Redness and warmth in the affected area
* Fatigue

If you suspect that you or someone you know may have spondylitis, ankylosing, it is important to seek medical attention for proper diagnosis and treatment. A healthcare professional can perform a physical examination and order imaging tests, such as X-rays or MRIs, to confirm the diagnosis and rule out other conditions.

Treatment for spondylitis, ankylosing typically involves a combination of medications and physical therapy. Medications may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy can help improve mobility and flexibility, as well as strengthen the muscles supporting the affected joints.

In severe cases of spondylitis, ankylosing, surgery may be necessary to repair or replace damaged joints. In some cases, the condition may progress to the point where the joints become fused and immobile, a condition known as ankylosis.

While there is no cure for spondylitis, ankylosing, early diagnosis and appropriate treatment can help manage symptoms and slow the progression of the disease. With proper care and support, individuals with spondylitis, ankylosing can lead active and fulfilling lives.

There are several types of JA, including:

1. Systemic juvenile idiopathic arthritis (SJIA): A severe form of JA that affects the entire body, causing fever, rash, and swollen lymph nodes in addition to joint inflammation.
2. Polyarticular juvenile idiopathic arthritis (PJIA): A common form of JA that affects multiple joints, especially in the hands and feet.
3. Oligoarticular juvenile idiopathic arthritis (OJIA): A mild form of JA that affects only a few joints.
4. Juvenile psoriatic arthritis (JPsA): A type of JA that is associated with psoriasis, a skin condition characterized by red, scaly patches.
5. Enthesitis-related juvenile idiopathic arthritis (ER-JIA): A rare form of JA that affects the areas where tendons and ligaments attach to bones.
6. Undifferentiated arthritis: A type of JA that does not fit into any of the other categories.

The symptoms of JA can vary depending on the specific type and severity of the condition, but may include:

* Joint pain and stiffness
* Swelling and redness in the affected joints
* Fatigue and fever
* Loss of mobility and range of motion
* Difficulty walking or standing

The exact cause of JA is not known, but it is believed to involve a combination of genetic and environmental factors. There is no cure for JA, but treatment options are available to help manage symptoms and prevent long-term joint damage. These may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying anti-rheumatic drugs (DMARDs), as well as physical therapy and lifestyle modifications.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

Examples of OIs include:

1. Pneumocystis pneumonia (PCP): A type of pneumonia caused by the fungus Pneumocystis jirovecii, which is commonly found in the lungs of individuals with HIV/AIDS.
2. Cryptococcosis: A fungal infection caused by Cryptococcus neoformans, which can affect various parts of the body, including the lungs, central nervous system, and skin.
3. Aspergillosis: A fungal infection caused by Aspergillus fungi, which can affect various parts of the body, including the lungs, sinuses, and brain.
4. Histoplasmosis: A fungal infection caused by Histoplasma capsulatum, which is commonly found in the soil and can cause respiratory and digestive problems.
5. Candidiasis: A fungal infection caused by Candida albicans, which can affect various parts of the body, including the skin, mouth, throat, and vagina.
6. Toxoplasmosis: A parasitic infection caused by Toxoplasma gondii, which can affect various parts of the body, including the brain, eyes, and lymph nodes.
7. Tuberculosis (TB): A bacterial infection caused by Mycobacterium tuberculosis, which primarily affects the lungs but can also affect other parts of the body.
8. Kaposi's sarcoma-associated herpesvirus (KSHV): A viral infection that can cause various types of cancer, including Kaposi's sarcoma, which is more common in individuals with compromised immunity.

The diagnosis and treatment of OIs depend on the specific type of infection and its severity. Treatment may involve antibiotics, antifungals, or other medications, as well as supportive care to manage symptoms and prevent complications. It is important for individuals with HIV/AIDS to receive prompt and appropriate treatment for OIs to help prevent the progression of their disease and improve their quality of life.

The exact cause of osteoarthritis is not known, but it is thought to be due to a combination of factors such as genetics, wear and tear on joints over time, and injuries or trauma to the joint. Osteoarthritis can affect any joint in the body, but it most commonly affects the hands, knees, hips, and spine.

The symptoms of osteoarthritis can vary depending on the severity of the condition and which joint is affected. Common symptoms include:

* Pain or tenderness in the joint
* Stiffness, especially after periods of rest or inactivity
* Limited mobility or loss of flexibility
* Grating or crackling sensations when the joint is moved
* Swelling or redness in the affected joint
* Muscle weakness or wasting

There is no cure for osteoarthritis, but there are several treatment options available to manage the symptoms and slow the progression of the disease. These include:

* Pain relief medications such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
* Physical therapy to improve mobility and strength
* Lifestyle modifications such as weight loss, regular exercise, and avoiding activities that exacerbate the condition
* Bracing or orthotics to support the affected joint
* Corticosteroid injections or hyaluronic acid injections to reduce inflammation and improve joint function
* Joint replacement surgery in severe cases where other treatments have failed.

Early diagnosis and treatment of osteoarthritis can help manage symptoms, slow the progression of the disease, and improve quality of life for individuals with this condition.

... is an antirheumatic agent. Iversen M, Munck J, Schourup K (1953). "On the toxicity of 3-hydroxy-2- ... Antirheumatic products, Quinolinols, Alpha hydroxy acids, All stub articles, Musculoskeletal system drug stubs). ...
It is an antirheumatic agent in veterinary medicine. It has attracted interest as an anticancer agent. Aminopropionitrile is ...
... is an antirheumatic agent developed from tiopronin. Activity is mediated by the two thiol groups that the molecule ... Antirheumatic products, Carboxylic acids, Propionamides, Thiols, All stub articles, Musculoskeletal system drug stubs). ...
Some cucurbitacins can be made anti-rheumatic agent. "Cucurbitaceae Cayaponia tayuya". International Plant Names Index. ...
... is a gold salt used as an antirheumatic agent. Perrier P, Raffoux C, Thomas P, Tamisier JN, Busson M, Gaucher A, ... levamisole and D-penicillamine as first choice slow-acting antirheumatic drugs in rheumatoid arthritis--a long-term follow-up ... Antirheumatic products, Metal-containing drugs, All stub articles, Musculoskeletal system drug stubs). ...
The main uses of mepacrine are as an antiprotozoal, antirheumatic, and an intrapleural sclerosing agent. Antiprotozoal use ... Antiprotozoal agents, Antimalarial agents, Sterilization (medicine), Experimental methods of birth control, Acridines, ... Agents Chemother. 55 (5): 1827-1830. doi:10.1128/aac.01296-10. PMC 3088196. PMID 21383088. Canete R, Escobedo AA, Gonzalez ME, ... As an intrapleural sclerosing agent, it is used as pneumothorax prophylaxis in patients at high risk of recurrence, e.g., ...
... is a gold salt classified by the World Health Organization as an antirheumatic agent. It has the brand name Ridaura. ... Antirheumatic products, Acetate esters, Metal-containing drugs, Gold-sulfur compounds, Disease-modifying antirheumatic drugs). ... the protozoan agent of human amebiasis. Assays of thioredoxin reductase and transcriptional profiling suggest that the effect ... International Journal of Antimicrobial Agents. 58 (5): 106425. doi:10.1016/j.ijantimicag.2021.106425. PMID 34419578. S2CID ...
... a toxic blistering agent once used as an exfoliating agent, anti-rheumatic drug and an aphrodisiac. The substance has also ... Cantharidin, the active agent, is a terpenoid, and is produced by some other insects, such as Epicauta immaculata. Cantharidin ... The beetle secretes the agent orally, and exudes it from its joints as a milky fluid. The potency of the insect as a blistering ... Note: the active agent appears variously as cantharidin,: 41 and "cantharadin": 43, 45ff or "canthariadin": 238 (sic). Aggrawal ...
Antimalarial agents, Antirheumatic products, Articles containing video clips, Chloroarenes, HERG blocker, Primary alcohols, ... Both agents also inhibit CYP2D6 activity and may interact with other medications that depend on this enzyme. Antimalarials are ... It enhances hypoglycemic effects of insulin and oral hypoglycemic agents. Dose altering is recommended to prevent profound ... "Fluorescence probe measurement of the intralysosomal pH in living cells and the perturbation of pH by various agents". ...
Antirheumatic products, Chelating agents, Enantiopure drugs, Human drug metabolites, Nephrotoxins, Non-proteinogenic amino ... It is used as a chelating agent: In Wilson's disease, a rare genetic disorder of copper metabolism, penicillamine treatment ... Penicillamine can be used as a disease-modifying antirheumatic drug (DMARD) to treat severe active rheumatoid arthritis in ... although it is rarely used today due to availability of TNF inhibitors and other agents, such as tocilizumab and tofacitinib. ...
"Studies on antirheumatic agents: 3-benzoylpropionic acid derivatives", Chem. Pharm. Bull., vol. 36, no. 6, pp. 2050-2060, doi: ...
The term is often used in contrast to nonsteroidal anti-inflammatory drugs (which refers to agents that treat the inflammation ... "Disease modifying antirheumatic drugs (DMARDs)". "antirheumatic" at Dorland's Medical Dictionary Buer, Jonas Kure (2015). "A ... Disease-modifying antirheumatic drugs (DMARDs) comprise a category of otherwise unrelated disease-modifying drugs defined by ... Nandi P, Kingsley GH, Scott DL (May 2008). "Disease-modifying antirheumatic drugs other than methotrexate in rheumatoid ...
975 Poisoning by agents primarily acting on the smooth and skeletal muscles and respiratory system 976 Poisoning by agents ... and antirheumatics 966 Poisoning by anticonvulsants and anti-Parkinsonism drugs 967 Poisoning by sedatives and hypnotics 968 ... the autonomic nervous system 972 Poisoning by agents primarily affecting the cardiovascular system 973 Poisoning by agents ... 962 Poisoning by hormones and synthetic substitutes 963 Poisoning by primarily systemic agents 964 Poisoning by agents ...
Prognosis of acquired immune deficiencies depends on avoiding or treating the causative agent or condition (like AIDS). ... disease-modifying antirheumatic drugs, immunosuppressive drugs after organ transplants, glucocorticoids) and environmental ... can result from various immunosuppressive agents, for example, malnutrition, aging, particular medications (e.g., chemotherapy ...
... adverse effects in therapeutic use E933 Primarily systemic agents causing adverse effects in therapeutic use E934 Agents ... at Unspecified place E849.0 Place of occurrence at home E850 Accidental poisoning by analgesics antipyretics and antirheumatics ... use E942 Agents primarily affecting the cardiovascular system causing adverse effects in therapeutic use E943 Agents primarily ... in therapeutic use E944 Water mineral and uric acid metabolism drugs causing adverse effects in therapeutic use E945 Agents ...
Its advantage over that drug in the treatment of ulcerative colitis is believed to be the delivery of the active agent past the ... It is in the category of disease-modifying antirheumatic drugs (DMARDs) family of medications. It is unclear exactly how it ...
Anti-inflammatory agents, Azetidines, Breakthrough therapy, COVID-19 drug development, Non-receptor tyrosine kinase inhibitors ... Pyrazoles, Pyrrolopyrimidines, Sulfonamides, Disease-modifying antirheumatic drugs). ...
It went out of interest until 1924 when it was noted as a chemotherapeutic agent for tuberculosis by Holger Møllgaard in ... Like several other gold compounds, this species is used as an antirheumatic. The first placebo-controlled trial was probably ... Shaw III CF (September 1999). "Gold-based therapeutic agents". Chemical Reviews. 99 (9): 2589-600. doi:10.1021/cr980431o. PMID ... Antirheumatic products, Metal-containing drugs, Gold-sulfur compounds, Aurates, All stub articles, Musculoskeletal system drug ...
Other agents which have been shown to reverse chloroquine resistance in malaria are chlorpheniramine, gefitinib, imatinib, ... Disease-modifying antirheumatic drugs). ... in pre-clinical models as a potential agent against chikungunya ... July 2012). "Sontochin as a guide to the development of drugs against chloroquine-resistant malaria". Antimicrobial Agents and ... Chloroquine is also a lysosomotropic agent, meaning it accumulates preferentially in the lysosomes of cells in the body.[ ...
The biologic agent rituximab (anti-B cell therapy) is now licensed for use in refractory rheumatoid arthritis.Physiotherapy is ... disease-modifying antirheumatic drugs), monoclonal antibodies, such as infliximab and adalimumab, the TNF inhibitor etanercept ...
Where this condition has been correctly diagnosed, various anti-rheumatic drugs as well as colchicine may be trialled to find ... achieved using intra-articular agents (chemical or radioactive) can provide good results, with efficacy reported for at least 1 ... Low-dose colchicine (and some other 'anti-rheumatic' therapies e.g. hydroxychloroquine) have been used with some success. (Use ...
It is considered a promising agent as it inhibits JAK1 selectively, similar to already marketed upadacitinib.[medical citation ... modifying anti‑rheumatic drugs (DMARDs). Filgotinib may be used as monotherapy or in combination with methotrexate (MTX). ... Who Have an Inadequate Response to Biologic Disease-modifying Anti-rheumatic Drug(s) (DMARDs) Treatment (FINCH 2)" at ... on Clinical Response in Patients With Moderate to Severe Rheumatoid Arthritis Refractory to Disease-Modifying Antirheumatic ...
... antirheumatic agents MeSH D27.505.954.329.030 - anti-inflammatory agents, non-steroidal MeSH D27.505.954.329.337 - gout ... antiviral agents MeSH D27.505.954.122.388.077 - anti-retroviral agents MeSH D27.505.954.122.388.077.088 - anti-hiv agents MeSH ... tocolytic agents MeSH D27.505.954.016 - anti-allergic agents MeSH D27.505.954.122 - anti-infective agents MeSH D27.505.954.122. ... tranquilizing agents MeSH D27.505.696.277.950.015 - anti-anxiety agents MeSH D27.505.696.277.950.025 - antimanic agents MeSH ...
Biological agents should generally be used only if methotrexate and other conventional agents are not effective after a trial ... Disease-modifying antirheumatic drugs (DMARDs), such as hydroxychloroquine and methotrexate, may be used to try to slow the ... The most commonly used agent is methotrexate with other frequently used agents including sulfasalazine and leflunomide. ... No infectious agent has been consistently linked with RA and there is no evidence of disease clustering to indicate its ...
He carried out research into the effect of salicin, an extract from willow bark and a known anti-rheumatic treatment. This work ... Stewart, William K.; Fleming, L. W. (1 October 1987). "Perthshire Pioneer of Anti-Inflammatory Agents". Scottish Medical ...
June 1995). "A comparative study of tenidap, a cytokine-modulating anti-rheumatic drug, and diclofenac in rheumatoid arthritis ... "Rationally designed multitarget agents against inflammation and pain". Current Medicinal Chemistry. 20 (13): 1783-99. doi: ...
In 1959 it became the eighth cytotoxic anticancer agent to be approved by the FDA. The abbreviation CP is common, although ... it remains an important treatment for life-threatening autoimmune diseases where disease-modifying antirheumatic drugs (DMARDs ... The main use of cyclophosphamide is with other chemotherapy agents in the treatment of lymphomas, some forms of brain cancer, ... Like other alkylating agents, cyclophosphamide is teratogenic and contraindicated in pregnant women (pregnancy category D) ...
... as its conjugate base is a chelating agent, with an affinity for iron(III). Salicylic acid slowly degrades to ... Salicylate's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory ... Aminosalicylic acid is used to induce remission in ulcerative colitis, and has been used as an antitubercular agent often ... Chelating agents, Monohydroxybenzoic acids, Nonsteroidal anti-inflammatory drugs, Plant hormones, World Health Organization ...
People who have previously been treated with an alkylating agent may have an excessive risk of cancers if treated with ... Being a disease-modifying antirheumatic drug (DMARD), azathioprine has been used for the management of the signs and symptoms ... It is also an important therapy and steroid-sparing agent for inflammatory bowel disease (such as Crohn's disease and ... agent. Azathioprine is also used to maintain remission in people who have granulomatosis with polyangiitis. It can be very ...
The natural history of a disease is sometimes said to start at the moment of exposure to causal agents. Knowledge of the ... Because these medications can alter the natural history of disease, they are referred to as disease-modifying antirheumatic ... This phase is defined by the host conditions, the disease agent (such as microorganisms and pathogens), and the environment. ... Benjamin, Onecia; Goyal, Amandeep; Lappin, Sarah L. (2022), "Disease Modifying Anti-Rheumatic Drugs (DMARD)", StatPearls, ...
... Anti-inflammatory and antirheumatic products is a therapeutic subgroup of the Anatomical Therapeutic Chemical ... ATC codes, Anti-inflammatory agents). ...
After the identification of B. burgdorferi as the causative agent of Lyme disease, antibiotics were selected for testing, ... Antibiotic-refractory Lyme arthritis may be symptomatically treated with NSAIDs, disease-modifying antirheumatic drugs (DMARDs ... Masuzawa T (December 2004). "Terrestrial distribution of the Lyme borreliosis agent Borrelia burgdorferi sensu lato in East ... November 2021). "mRNA vaccination induces tick resistance and prevents transmission of the Lyme disease agent". Science ...
Similarly, one might argue that the class of disease-modifying anti-rheumatic drugs (DMARD) is composed by one element (" ... and not all drugs used to treat atherosclerosis are triglyceride-lowering agents. A drug class is typically defined by a ... Nonsteroidal anti-inflammatory drug (NSAID) Disease-modifying antirheumatic drug (DMARD) Other systems of drug classification ... "disease-modifying") that albeit vaguely designates a mechanism of action, and one element ("anti-rheumatic drug") that ...
Cecilia Giampietro; Bruno Fautrel (2012). "Review Article: Anti-Interleukin-1 Agents in Adult Onset Still's Disease". ... in a group of 12 patients treated with anakinra than in a group of 10 patients taking other disease-modifying antirheumatic ...
Medications used to treat the progression of the disease include the following: Disease-modifying antirheumatic drugs (DMARDs) ... Medications used include NSAIDs, steroids, DMARDs such as sulfasalazine, and biologic agents such as TNF inhibitors. ...
... is used to treat adults with moderate to severe rheumatoid arthritis (RA) as a second-line agent, and as a first-line ... Disease-modifying antirheumatic drugs). ... agent for people whose RA is severe and rapidly progressing. It ...
ISBN 978-0-9805790-9-3. Berners-Price SJ, Filipovska A (September 2011). "Gold compounds as therapeutic agents for human ... is a gold compound that is used for its immunosuppressive anti-rheumatic effects. Along with an orally-administered gold salt, ... Antirheumatic products, Metal-containing drugs, Organic sodium salts, Thiolates, Gold-sulfur compounds, French inventions, ...
Auranofin Shaw, III C. F. (1999). "Gold-Based Therapeutic Agents". Chemical Reviews. 99 (9): 2589-600. doi:10.1021/cr980431o. ... Antirheumatic products, Organosulfur compounds, Metal-containing drugs, Gold-sulfur compounds). ...
Infectious agents are considered T cell activators, a step needed for activation of autoimmune diseases. These mechanisms are ... to reduce inflammation Glucocorticoids to reduce inflammation Disease-modifying anti-rheumatic drugs (DMARDs) to decrease the ... Due to the fact symptoms vary for affected location, disease causing agents, and individuals, it is difficult for proper ... Wucherpfennig KW (October 2001). "Mechanisms for the induction of autoimmunity by infectious agents". The Journal of Clinical ...
It is a very active anti-angiogenic agent and also acts as an immunomodulator. Pomalidomide was approved in February 2013 by ... Bermas BL (April 2020). "Paternal safety of anti-rheumatic medications". Best Practice & Research. Clinical Obstetrics & ... Hofland P (December 2013). "Reversal of Fortune: How a Vilified Drug Became a Life-saving Agent in the "War" Against Cancer". ... It may interact with sedatives due to its sedative action and bradycardic agents, like beta-blockers, due to its bradycardia- ...
Agents Classified by the IARC Monographs, Volumes 1-110 Archived 25 October 2011 at the Wayback Machine IARC Working Group on ... Disease-modifying antirheumatic drugs). ... a new antilymphocytic agent". Agents and Actions. 6 (4): 468-75 ... Ciclosporin has been investigated as a possible neuroprotective agent in conditions such as traumatic brain injury, and has ...
... and antimicrobial agent, also used for the removal of parasites diphenhydramine - histamine blocker doxycycline - antibiotic, ... anti-inflammatory and antirheumatic Telazol - intravenous drug used to induce anesthesia; combination of tiletamine and ... reversal agent for benzodiazepines flunixin meglumine - nonsteroidal anti-inflammatory drug used as an analgesic and ... combination anesthetic agent chloramphenicol - antibacterial used to treat anaerobic bacterial infections, both Gram-positive ...
In vivo and in vitro studies of encapsulated alpha-1-antitrypsin and corticosteroids as anti-rheumatic agents. Pitt, E. (Author ... In vivo and in vitro studies of encapsulated alpha-1-antitrypsin and corticosteroids as anti-rheumatic agents ...
... strategies such as tapering and withdrawal of disease-modifying antirheumatic drugs (DMARDs) are being investigated. In several ... Antirheumatic Agents / administration & dosage* * Arthritis, Rheumatoid / diagnosis * Arthritis, Rheumatoid / drug therapy* * ... strategies such as tapering and withdrawal of disease-modifying antirheumatic drugs (DMARDs) are being investigated. In several ...
Immunosuppressive Agents. Immunologic Factors. Physiological Effects of Drugs. Antirheumatic Agents. Antineoplastic Agents, ... Antitubercular Agents. Anti-Bacterial Agents. Anti-Infective Agents. Enzyme Inhibitors. Antifungal Agents. ... Alkylating Agents. Molecular Mechanisms of Pharmacological Action. Antineoplastic Agents. Myeloablative Agonists. Antibiotics, ...
Dermatologic Agents. Enzyme Inhibitors. Folic Acid Antagonists. Immunosuppressive Agents. Immunologic Factors. Antirheumatic ... Abortifacient Agents, Nonsteroidal. Abortifacient Agents. Reproductive Control Agents. Physiological Effects of Drugs. ... T1-weighted images were acquired before and after the administration of intravenous contrast agent containing gadolinium. ... T1-weighted images were acquired before and after the administration of intravenous contrast agent containing gadolinium. ...
Shop Humira®, Injection, Adalimumab, AbbVie Inc, 40 mg / 0.4 mL Disease-Modifying Antirheumatic Agent ...
Clinically used antirheumatic agent auranofin is a proteasomal deubiquitinase inhibitor and inhibits tumor growth. Oncotarget. ...
Anti-Inflammatory Agents, Antirheumatic Agents, and Inflammation Mediators. Anti-Inflammatory Agents. Antibiotics, Glycopeptide ... Antineoplastic and Immunosuppressive Agents. Antineoplastic Agents. Antirheumatic Agents, Gold. Antirheumatic Agents. Diuretics ...
Categories: Anti-Inflammatory Agents, Antirheumatic Agents, and Inflammation Mediators Image Types: Photo, Illustrations, Video ...
A61P29/00-Non-central analgesic, antipyretic or antiinflammatory agents, e.g. antirheumatic agents; Non-steroidal ... A kind of external washout with traditional Chinese herbs agent treating wind heat blood-dryness type seborrheic dermatitis of ...
Concomitant Use with Other Biologic Agents and Disease Modifying Antirheumatic Drugs (DMARDs) in GPA and MPA ... Limited data are available on the safety of the use of biologic agents or DMARDs. Observe patients closely for signs of ... Non-progressing (including stable disease), low-grade, CD20-positive, B-cell NHL as a single agent after first line ... Relapsed or refractory, low-grade or follicular, CD20-positive, B-cell NHL as a single agent. ...
Efficacy, tolerability and cost effectiveness of disease-modifying antirheumatic drugs and biologic agents in rheumatoid ... It is well know that the progression of radiological changes is slowed by the use of disease-modifying antirheumatic agents ( ... Biological agents: a novel approach to the therapy of rheumatoid arthritis. Expert Opinion on Investigational Drugs, 2000, 9(7 ... Are biologics more effective than classical disease-modifying antirheumatic drugs? Arthritis Research and Therapy, 2008, 10(5): ...
2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents ... Based on the 2012 American College of Rheumatology guidelines, individuals who are being considered for biologic agent ...
exp immunosuppressive agent/ OR exp antirheumatic agent/ OR exp Monoclonal antibody/ OR (Glucocorticoid* OR Corticosteroid* OR ... exp immunosuppressive agents/ OR exp antirheumatic agents/ OR exp Antibodies, Monoclonal/ OR (Glucocorticoid* OR Corticosteroid ... mh "Immunosuppressive Agents"] OR [mh "Antirheumatic Agents"] OR [mh "Antibodies, Monoclonal"] OR (Glucocorticoid* OR ... OR Glucocorticosteroid* OR antirheumatic drug* OR antirheumatic agent* OR anti-inflammator* OR DMARDS OR Methotrexate OR MTX OR ...
Graudal N, Jürgens G. Similar effects of disease-modifying antirheumatic drugs, glucocorticoids, and biologic agents on ... Down titration and discontinuation strategies of tumor necrosis factor blocking agents for rheumatoid arthritis in patients ... as well as any change in the use of glucocorticoids or disease modifying antirheumatic drugs (DMARDs), and the occurrence of ...
... and often combined immunosuppressive and antiinflammatory agents, including the new biological disease-modifying antirheumatic ...
Antirheumatic Agents Entry term(s). Agent, Anti-Rheumatic Agent, Antirheumatic Anti Rheumatic Agent Anti Rheumatic Agents Anti ... Agent, Anti-Rheumatic. Agent, Antirheumatic. Anti Rheumatic Agent. Anti Rheumatic Agents. Anti Rheumatic Agents, Non Steroidal ... Anti Rheumatic Drugs Anti-Rheumatic Agent Anti-Rheumatic Agents Anti-Rheumatic Drug Anti-Rheumatic Drugs Antirheumatic Agent ... Anti Rheumatic Drug. Anti Rheumatic Drugs. Anti-Rheumatic Agent. Anti-Rheumatic Agents. Anti-Rheumatic Agents, Non-Steroidal. ...
Antirheumatic Agents 6% * Self Efficacy 6% * Medical Errors 5% * Direction compound 5% ...
Antirheumatic Agents 10% * Inflammation 10% * Pathogenesis of giant cell arteritis with focus on cellular populations. Stamatis ...
All had biopsy-proven pulmonary sarcoidosis, and all required additional disease-modifying antirheumatic drugs for adequate ... often requiring anti-tumor necrosis factor a agents. Further studies are needed to determine the generalizability of these ... inadequately responsive to conventional oral disease-modifying antirheumatic drugs, ... control (stepwise progression from hydroxychloroquine to methotrexate to anti-tumor necrosis factor a agents) of their joint ...
... of RA and the capability of biologically engineered treatments for RA have expanded the armamentarium of antirheumatic agents. ... of RA and the capability of biologically engineered treatments for RA have expanded the armamentarium of antirheumatic agents. ... of RA and the capability of biologically engineered treatments for RA have expanded the armamentarium of antirheumatic agents. ... of RA and the capability of biologically engineered treatments for RA have expanded the armamentarium of antirheumatic agents. ...
Limited data are available on the safety of the use of biologic agents or disease modifying antirheumatic drugs (DMARDs) other ... Comment: Myelosuppressive agents can produce additive myelosuppression. Avoid use and monitor patients receiving the ... Comment: Myelosuppressive agents can produce additive myelosuppression. Avoid use and monitor patients receiving the ... Immunosuppressive therapies, including irradiation, antimetabolites, alkylating agents, cytotoxic drugs and corticosteroids ( ...
Immunity against mycobacterium tuberculosis and risk of biological anti-rheumatic agents]. Yasui, Kozo. ... Thalidomide as an immunotherapeutic agent: the effects on neutrophil-mediated inflammation. Yasui, Kozo; Kobayashi, Norimoto; ...
1) P. Bertschinger, G. F. Zala and M. Fried, "Effect of Nonsteroidal Antirheumatic Agents on the Gastrointestinal Tract: ... Cytotoxic Agents.. The most commonly used cytotoxic drugs are azathioprine (Imuran), cyclophosphamide (Cytoxan) and cyclosporin ... Gold Salts. Intramuscular gold salts were, until the 1990s, the most often used DMARD agents. They are rarely used now due to ... DMARDs stands for disease modifying anti rheumatic drugs.. DMARDs used to not be used for arthritis except as a last resort. ...
Antirheumatic agents.. 650 02 - SUBJECT ADDED ENTRY--TOPICAL TERM. Topical term or geographic name as entry element. Arthritis ...
Salvage therapy was defined as an antirheumatoid drug, such as disease-modifying antirheumatic drugs, non-steroidal anti- ... inflammatory drugs and any biological agent for the treatment of RA, received on or after the day of the first dose of study ... cost of these medications creates a major barrier that limits universal access to these effective therapeutic agents. This has ...
Antirheumatic Agent 46% * Myorelaxant Agent 45% * Adrenal Cortex Hormone 38% * Tricyclic Antidepressant Agent 20% ...
Lee, Y. C., Chiu, H. M., Chiang, T. H., Yen, A. M. F., Chiu, S. Y. H., Chen, S. L. S., Fann, J. C. Y., Yeh, Y. P., Liao, C. S., Hu, T. H., Tu, C. H., Tseng, P. H., Chen, C. C., Chen, M. J., Liou, J. M., Liao, W. C., Lai, Y. P., Wang, C. P., Ko, J. Y., Wang, H. P., & 4 othersChiang, H., Lin, J. T., Chen, H. H. & Wu, M. S., 2013, In: BMJ Open. 3, 10, e003989.. Research output: Contribution to journal › Article › peer-review ...
Antirheumatic Agents Medicine & Life Sciences 33% * Autoantibodies Medicine & Life Sciences 24% * Lymphocyte Function- ...
  • As more patients with established rheumatoid arthritis (RA) achieve remission or low disease activity, strategies such as tapering and withdrawal of disease-modifying antirheumatic drugs (DMARDs) are being investigated. (nih.gov)
  • Results/conclusions: At present, a common strategy for the treatment of RA uses methotrexate either as monotherapy or in combination with a variety of conventional and/or biologic disease-modifying antirheumatic drugs (DMARDs), with the goal of inducing remission of active disease. (nebraska.edu)
  • These are called disease-modifying antirheumatic drugs (DMARDs). (medlineplus.gov)
  • Biologic DMARDs such as anti-TNF agents, IL-1 inhibitors and IL-6 inhibitors. (medlineplus.gov)
  • It is well know that the progression of radiological changes is slowed by the use of disease-modifying antirheumatic agents (DMARD) [5] and can be ameliorated by the use of biologic agents [6-8]. (who.int)
  • Based on the 2012 American College of Rheumatology guidelines, individuals who are being considered for biologic agent immunosuppression, including tumor necrosis factor antagonists, should be screened prior to starting biologic therapy. (medscape.com)
  • All had biopsy-proven pulmonary sarcoidosis, and all required additional disease-modifying antirheumatic drugs for adequate control (stepwise progression from hydroxychloroquine to methotrexate to anti-tumor necrosis factor a agents) of their joint manifestations. (cdc.gov)
  • Their arthritis is chronic and, unlike arthritis in non-WTC-exposed sarcoid patients, inadequately responsive to conventional oral disease-modifying antirheumatic drugs, often requiring anti-tumor necrosis factor a agents. (cdc.gov)
  • At the same time my doctor was also suggesting I take methotrexate, which is a chemotherapy agent. (conqueringarthritis.com)
  • T1-weighted images were acquired before and after the administration of intravenous contrast agent containing gadolinium. (clinicaltrials.gov)
  • It is provided as an additional code where it is desired to identify the bacterial agent in diseases classified elsewhere. (cdc.gov)
  • Aspirin, the nonsteroidal antiinflammatory agents and corticosteroids are used commonly in these conditions, but have little effect in altering the natural history and outcomes of inflammatory arthritis, which can lead to cartilage and joint destruction and severe disability. (nih.gov)
  • Disease-modifying antirheumatic drugs (DMARDs) can retard or prevent disease progression and, thus, joint destruction and subsequent loss of function. (medscape.com)
  • All had biopsy-proven pulmonary sarcoidosis, and all required additional disease-modifying antirheumatic drugs for adequate control (stepwise progression from hydroxychloroquine to methotrexate to anti-tumor necrosis factor a agents) of their joint manifestations. (cdc.gov)
  • Their arthritis is chronic and, unlike arthritis in non-WTC-exposed sarcoid patients, inadequately responsive to conventional oral disease-modifying antirheumatic drugs, often requiring anti-tumor necrosis factor a agents. (cdc.gov)
  • Prevalence may be decreasing with the advent of more potent antirheumatic agents. (medscape.com)
  • The term "antirheumatic drugs" refers to agents used in the therapy of inflammatory arthritis, predominantly rheumatoid arthritis, but also idiopathic juvenile arthritis, psoriatic arthritis, ankylosing spondylitis and others. (nih.gov)
  • Immunosuppressive/cytotoxic drugs are used as steroid-sparing agents for the muscle disease of dermatomyositis. (medscape.com)
  • It is well know that the progression of radiological changes is slowed by the use of disease-modifying antirheumatic agents (DMARD) [5] and can be ameliorated by the use of biologic agents [6-8]. (who.int)
  • These important agents include the tumor necrosis factor antagonists, anticytokines (such as anakinra) and other major immunosuppressive agents (rituximab, abatacept, and tocilizumab). (nih.gov)
  • RÉSUMÉ La fréquence des modifications radiologiques au niveau des mains et des pieds a été étudiée au sein d'une population hospitalière bien définie constituée de patients atteints de polyarthrite rhumatoïde, à Jeddah en Arabie saoudite. (who.int)
  • Safe use of antirheumatic agents in patients with comorbidities. (medscape.com)